Atherosclerosis最新文献

{"title":"Making the invisible visible: Leveraging electronic health records to uncover familial hypercholesterolemia in primary care","authors":"Meral Kayikcioglu","doi":"10.1016/j.atherosclerosis.2025.120454","DOIUrl":"10.1016/j.atherosclerosis.2025.120454","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120454"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond stenosis: Is CT enough to assess the vulnerable carotid plaque?","authors":"Edoardo Conte MD","doi":"10.1016/j.atherosclerosis.2025.120422","DOIUrl":"10.1016/j.atherosclerosis.2025.120422","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"408 ","pages":"Article 120422"},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2025 focused update of the 2019 ESC/EAS guidelines for the management of dyslipidemias - Advancing evidence-based care through innovation.","authors":"Florian Kronenberg, Jan Borén, Kausik K Ray","doi":"10.1016/j.atherosclerosis.2025.120487","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.120487","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120487"},"PeriodicalIF":5.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias.","authors":"François Mach, Konstantinos C Koskinas, Jeanine E Roeters van Lennep, Lale Tokgözoğlu, Lina Badimon, Colin Baigent, Marianne Benn, Christoph J Binder, Alberico L Catapano, Guy G De Backer, Victoria Delgado, Natalia Fabin, Brian A Ference, Ian M Graham, Ulf Landmesser, Ulrich Laufs, Borislava Mihaylova, Børge Grønne Nordestgaard, Dimitrios J Richter, Marc S Sabatine","doi":"10.1016/j.atherosclerosis.2025.120479","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.120479","url":null,"abstract":"","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120479"},"PeriodicalIF":5.7,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Twist1 promoting neointima hyperplasia after vascular injury in diabetes via regulating hyperglycemia-induced phenotype switching of vascular smooth muscle cells","authors":"Yaoling Wang ,&nbsp;Kang Yang ,&nbsp;Gege Jiang ,&nbsp;Xichuan Zheng ,&nbsp;Fang Cheng ,&nbsp;Wei Li","doi":"10.1016/j.atherosclerosis.2025.120496","DOIUrl":"10.1016/j.atherosclerosis.2025.120496","url":null,"abstract":"<div><h3>Background and aims</h3><div>Neointimal hyperplasia is a key pathology in Type 2 Diabetes Mellitus (T2DM) vascular complications. It involves phenotypic switching of vascular smooth muscle cells (VSMCs) triggered by hyperglycemia, though the exact mechanisms remain unclear.</div></div><div><h3>Methods</h3><div>We employed Twist1 vascular smooth muscle-specific knockout mice with carotid artery ligation in a T2DM model to study Twist1's role in diabetic neointimal hyperplasia. In vitro, we examined how hyperglycemia via Pkcβ/Ikkβ/Nf-κb pathway affects Twist1's regulation of contractile proteins, matrix molecules, cell morphology, migration, and proliferation in rat VSMCs using Western blotting, immunofluorescence, wound healing assays, and EdU incorporation. Co-immunoprecipitation and colocalization assessed how Twist1-p300 interaction under high glucose affects Myocardin-Srf binding.</div></div><div><h3>Results</h3><div>Twist1 was significantly upregulated in VSMCs of T2DM mice. Vascular smooth muscle-specific Twist1 knockout reduced neointimal formation after vascular injury in T2DM. High glucose activated Pkcβ/Ikkβ/Nf-κb pathway, promoting Twist1 upregulation and nuclear translocation, decreasing contractile protein expression while increasing matrix molecules and VSMC proliferation/migration. Mechanistically, upregulated Twist1 increased p300 binding, blocking p300's transcriptional co-activation of Myocardin/Srf and inhibiting contractile gene transcription in VSMCs.</div></div><div><h3>Conclusions</h3><div>Hyperglycemia activates the PKCβ/IKKβ/NF-κB pathway, upregulating Twist1 and promoting its nuclear translocation. Twist1 binding to p300 inhibits Myocardin/SRF-mediated contractile gene transcription, leading to VSMC phenotypic switching and neointimal hyperplasia. These findings highlight Twist1 as a potential therapeutic target for diabetic vascular complications.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120496"},"PeriodicalIF":5.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding MASLD — from molecular pathogenesis to cardiovascular risk: A concise review for the clinical cardiologist","authors":"Carlo Ratti ,&nbsp;Mattia Malaguti ,&nbsp;D'Aniello Emanuele ,&nbsp;Antonio Bellasi ,&nbsp;Gianluca Sanna","doi":"10.1016/j.atherosclerosis.2025.120495","DOIUrl":"10.1016/j.atherosclerosis.2025.120495","url":null,"abstract":"<div><h3>Background and aims</h3><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently replaced non-alcoholic fatty liver disease (NAFLD) as the preferred nomenclature, reflecting a shift toward inclusion-based diagnostic criteria rooted in metabolic dysfunction. Beyond its hepatic implications, MASLD has emerged as an independent, modifiable driver of cardiovascular disease (CVD).</div></div><div><h3>Methods</h3><div>This review summarizes and synthesizes robust epidemiological and mechanistic evidence linking MASLD to cardiovascular outcomes.</div></div><div><h3>Results</h3><div>MASLD is associated with increased risk of coronary artery disease, myocardial infarction, atrial fibrillation, stroke, and heart failure—particularly heart failure with preserved ejection fraction (HFpEF). Shared pathophysiological mechanisms include insulin resistance, chronic inflammation, oxidative stress, endothelial dysfunction, and atherogenic dyslipidemia, which collectively contribute to both hepatic fibrogenesis and vascular injury. Fibrosis stage, the strongest predictor of hepatic outcomes, also correlates with subclinical atherosclerosis and cardiovascular mortality, yet remains unaccounted for in current CVD risk models. Non-invasive fibrosis markers such as FIB-4 and elastography, originally developed for hepatology, are gaining traction in cardiovascular risk stratification. Furthermore, pharmacologic agents such as GLP-1 receptor agonists and SGLT2 inhibitors demonstrate dual efficacy in improving hepatic, metabolic, and cardiovascular outcomes.</div></div><div><h3>Conclusions</h3><div>This review provides an updated synthesis for cardiologists, outlining the evolution of MASLD nomenclature, its systemic pathophysiology, and its clinical implications—underscoring the urgent need for integrated, multidisciplinary management of this underrecognized cardiometabolic disease.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120495"},"PeriodicalIF":5.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144907900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac macrophages and their functions in homeostasis and injury","authors":"Giulia Trimaglio ,&nbsp;Peter Mirtschink ,&nbsp;Ali El-Armouche ,&nbsp;Triantafyllos Chavakis","doi":"10.1016/j.atherosclerosis.2025.120480","DOIUrl":"10.1016/j.atherosclerosis.2025.120480","url":null,"abstract":"<div><div>Due to their remarkable plasticity, macrophages can adapt to diverse environments and challenges therein, thereby exerting tissue-specific and context-specific functions. Macrophages are the most frequent immune cell population present in the heart and contribute substantially to cardiac homeostasis and function. Moreover, macrophages are key regulators throughout all stages of heart injury, acquiring diverse phenotypes that can either ameliorate or exacerbate cardiac pathology in a context-dependent manner. The contribution of macrophages to both tissue damage as well as to recovery/tissue repair during heart injury provides avenues for therapeutic modulation of their functions to beneficially influence heart injury progression and hence prevent heart failure. However, to effectively fine-tune macrophage function, a deep understanding of their heterogeneity is required. The present review focuses on the phenotypic diversity and different roles of macrophages in cardiac homeostasis as well as in ischemic and non-ischemic heart disease, and discusses macrophages as potential therapeutic targets in the settings of heart injury.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120480"},"PeriodicalIF":5.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144996285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in cholesterol levels among prepubertal children.","authors":"Jan Kafol, Mia Becker, Barbara Cugalj Kern, Jaka Sikonja, Matej Mlinaric, Katarina Sedej, Matej Kafol, Ana Drole Torkar, Jernej Kovac, Tadej Battelino, Urh Groselj","doi":"10.1016/j.atherosclerosis.2025.120484","DOIUrl":"https://doi.org/10.1016/j.atherosclerosis.2025.120484","url":null,"abstract":"<p><strong>Background and aims: </strong>Sex differences in cholesterol levels are well documented in adults and adolescents, but limited data exist for prepubertal children. This study aimed to evaluate innate sex differences in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels among prepubertal children, both in the general population and among those with familial hypercholesterolemia (FH).</p><p><strong>Methods: </strong>This cross-sectional study used data from Slovenia's Universal FH Screening Program. Two population-based random samples of children undergoing routine cholesterol screening at age 5 years were included from 2014 (N = 3412) and 2023 (N = 4182). In addition, a referred cohort from the Slovenian Hypercholesterolemia Registry (n = 1160, aged <10 years) who underwent genetic testing was analyzed.</p><p><strong>Results: </strong>In both the 2014 and 2023 cohorts, girls had significantly higher TC levels than boys (median difference: 0.10-0.11 mmol/L; p < 0.05). Among FH-negative children in the Registry, girls had on average 0.14 mmol/L higher TC and 0.13 mmol/L higher LDL-C than boys (both p < 0.05). No sex differences were observed in FH-positive children (p = 0.83 for TC; p = 0.82 for LDL-C). In the overall Registry cohort, after adjusting for FH status, girls had 0.11 mmol/L higher TC and 0.10 mmol/L higher LDL-C (both p < 0.05).</p><p><strong>Conclusion: </strong>Prepubertal girls have modestly higher TC and LDL-C than boys, a difference not observed in prepubertal FH-positive children, suggesting that the presence of a pathogenic FH variant may override innate physiological differences in lipid metabolism. These findings support universal early cholesterol screening and suggest that sex-specific reference values may improve early cardiovascular risk assessment in prepubertal FH-negative children.</p>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":" ","pages":"120484"},"PeriodicalIF":5.7,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of salivary inflammatory non coding RNA biomarkers for coronary artery disease through epicardial adipose tissue gene network analysis","authors":"Anandhi Sekar Arthi Sri ,&nbsp;Vishnu Priya Veeraraghavan ,&nbsp;Shankargouda Patil ,&nbsp;A. Thirumal Raj","doi":"10.1016/j.atherosclerosis.2025.120486","DOIUrl":"10.1016/j.atherosclerosis.2025.120486","url":null,"abstract":"<div><h3>Background and aim</h3><div>Epicardial adipose tissue (EAT), due to its proximity to the myocardium, contributes inflammatory profile in CAD onset and progression. Emerging evidence highlights the role of EAT-derived non-coding RNAs in modulating disease pathways. However, identifying EAT-specific biomarkers remains challenging for routine diagnosis. Therefore, this study aimed to identify non-invasive, multi-source biomarkers from EAT, plasma, and saliva, and their regulatory miRNAs and lncRNAs, through network analysis, regulatory mapping, and experimental validation.</div></div><div><h3>Methods</h3><div>Differential expression analyses identified upregulated genes and miRNAs in EAT. Protein interaction network was constructed for overlapping upregulated genes and downregulated miRNA targets along with inflammatory-related genes. Clustering, ontology, and topological analyses were performed to pinpoint hub biomarkers and regulatory non-coding RNAs. Key candidate molecules were then experimentally validated using saliva and plasma samples from a cohort of CAD patients (n = 30) and healthy controls (n = 30).</div></div><div><h3>Results</h3><div>A total of 840 upregulated and 1817 downregulated genes were identified in EAT with 36 upregulated and 82 downregulated miRNAs. Among 343 overexpressed inflammatory genes, CD8A, IL7R, and CCL5 emerged as hub biomarkers. Regulatory analysis uncovered 18 miRNAs and 548 lncRNAs influencing these hubs. Notably, hsa-miR-582–3p exhibited the highest number of lncRNA interactions and was significantly downregulated in saliva and plasma of CAD patients (<em>p</em> &lt; 0.05).</div></div><div><h3>Conclusions</h3><div>Our study establishes a link between EAT inflammation and salivary expression profiles, highlighting hsa-miR-582–3p as a promising non-invasive salivary biomarker for CAD. This integrative approach provides a valuable foundation for developing multi-source diagnostics in cardiovascular clinical settings.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120486"},"PeriodicalIF":5.7,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144866461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antiplatelet therapy with clopidogrel versus aspirin in atherosclerotic cardiovascular disease: a systematic review and meta-analysis","authors":"Maximilian Tscharre ,&nbsp;David Mutschlechner ,&nbsp;Kurt Huber ,&nbsp;Thomas Gremmel","doi":"10.1016/j.atherosclerosis.2025.120478","DOIUrl":"10.1016/j.atherosclerosis.2025.120478","url":null,"abstract":"<div><h3>Background and aims</h3><div>Whether single antiplatelet therapy (SAPT) with clopidogrel offers superior ischemic efficacy and a more favourable bleeding profile than aspirin in atherosclerotic cardiovascular disease is unclear.</div></div><div><h3>Methods</h3><div>A systematic search on the main databases Medline, Web of Science, and Embase until April 21, 2024 was performed. Only randomized trials were eligible for this analysis. As primary endpoint we analyzed major adverse cardiovascular events (MACE), defined as a composite of all-cause mortality, non-fatal myocardial infarction (MI) and non-fatal stroke. As secondary endpoints we investigated the individual primary endpoints as well as the rate of total and severe bleeding events. The analysis was carried out using the odds ratio (OR) as outcome measure. Due to the expected heterogeneity across studies, a random-effects model was fitted to the data.</div></div><div><h3>Results</h3><div>In total, 6 randomized trials comprising 33,508 patients (16,824 on clopidogrel, 16,684 on aspirin) were analyzed. Clopidogrel as compared to aspirin significantly reduced MACE (OR 0.85 [95 %CI 0.77–0.94], p &lt; 0.001, I² = 26 %). The reduction was driven by a decrease in non-fatal MI (OR 0.73 [95 %CI 0.60–0.90], p = 0.01, I² = 28 %) and stroke (OR 0.86 [95 %CI 0.74–1.00], p = 0.05, I² = 8 %), without increasing the rates of total (OR 1.04 [95 %CI 0.83–1.31], p = 0.73, I² = 72 %) or severe bleeding (OR 0.89 [95 %CI 0.83–1.18], p = 0.43, I² = 50 %). No effect on all-cause mortality was detectable (OR 0.96 [95 %CI 0.87–1.06], p = 0.41, I² = 0 %).</div></div><div><h3>Conclusion</h3><div>In patients with atherosclerotic cardiovascular disease, SAPT with clopidogrel is associated with lower MACE rates as compared to aspirin without increasing the risk of bleeding.</div></div>","PeriodicalId":8623,"journal":{"name":"Atherosclerosis","volume":"409 ","pages":"Article 120478"},"PeriodicalIF":5.7,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144880160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}